Download High-frequency oscillatory ventilation — a clinical approach

pg 10-24 q5
8/8/05
2:09 PM
Page 15
28. Ram F, Picot J, Lightowler J, Wedzicha J. Non-invasive positive pressure ventilation for
treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary
disease. Cochrane Database Syst Rev 2004; 3: CD004104.
46. Gomez-Merino E, Bach JR. Duchenne muscular dystrophy: prolongation of life by
noninvasive ventilation and mechanically assisted coughing. Am J Phys Med Rehabil
2002; 81: 411-415.
29. Brochard L. Non-invasive ventilation for acute exacerbations of COPD: a new standard of
care. Thorax 2000; 55: 817-818.
47. Crane SD, Elliott MW, Gilligan P, Richards K, Gray AJ. Randomised controlled comparison
of continuous positive airways pressure, bilevel non-invasive ventilation, and standard
treatment in emergency department patients with acute cardiogenic pulmonary oedema.
Emerg Med J 2004; 21: 155-161.
30. Carlucci A, Delmastro M, Rubini F, Fracchia C, Nava S. Changes in the practice of noninvasive ventilation in treating COPD patients over 8 years. Intensive Care Med 2003; 29:
419-425.
31. Conti G, Costa R, Craba A, Festa V, Catarci S. Non-invasive ventilation in COPD patients.
Minerva Anestesiol 2004; 70: 145-150.
34. Peter JV, Moran JL, Phillips-Hughes J, Warn D. Noninvasive ventilation in acute
respiratory failure – a meta-analysis update. Crit Care Med 2002; 30: 555-562.
35. Ram F, Wellington S, Rowe B, Wedzicha J. Non-invasive positive pressure ventilation for
treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane
Database Syst Rev 2005; 25(1): CD004360.
36. Efrati O, Modan-Moses D, Barak A, et al. Long-term non-invasive positive pressure
ventilation among cystic fibrosis patients awaiting lung transplantation. Isr Med Assoc J
2004; 6: 527-530.
37. Fauroux B, Hart N, Lofaso F. Non invasive mechanical ventilation in cystic fibrosis:
physiological effects and monitoring. Monaldi Arch Chest Dis 2002; 57: 268-272.
38. Moran F, Bradley J. Non-invasive ventilation for cystic fibrosis. Cochrane Database Syst
Rev 2003; 2: CD002769.
39. Serra A, Polese G, Braggion C, Rossi A. Non-invasive proportional assist and pressure
support ventilation in patients with cystic fibrosis and chronic respiratory failure. Thorax
2002; 57: 50-54.
40. Baydur A, Layne E, Aral H, et al. Long term non-invasive ventilation in the community
for patients with musculoskeletal disorders: 46 year experience and review. Thorax 2000;
55: 4-11.
41. Dettenmeier PA, Jackson NC. Chronic hypoventilation syndrome: treatment with noninvasive mechanical ventilation. AACN Clin Issues Crit Care Nurs 1991; 2: 415-431.
42. Simonds AK. Nasal intermittent positive pressure ventilation in neuromuscular and chest
wall disease. Monaldi Arch Chest Dis 1993; 48: 165-168.
43. Tzeng A, Bach J. Prevention of pulmonary morbidity for patients with neuromuscular
disease. Chest 2000; 118: 1390-1396.
44. Bach JR, Alba AS, Saporito LR. Intermittent positive pressure ventilation via the mouth
as an alternative to tracheostomy for 257 ventilator users. Chest 1993; 103: 174-182.
45. Ishikawa Y, Bach JR. Nocturnal respiratory failure as an indication of noninvasive
ventilation in the patient with neuromuscular disease. Respiration 1998; 65: 226.
50. Masip J, Betbese AJ, Paez JF, et al. Non-invasive pressure support ventilation versus
conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomised trial.
Lancet 2000; 356: 2126-2132.
51. Minuto A, Giacomini M, Giamundo B, et al. Non-invasive mechanical ventilation in
patients with acute cardiogenic pulmonary edema. Minerva Anestesiol 2003; 69: 835-838,
838-840.
52. Murray S. Bi-level positive airway pressure (BiPAP) and acute cardiogenic pulmonary
oedema (ACPO) in the emergency department. Aust Crit Care 2002; 15: 51-63.
53. Valipour A, Cozzarini W, Burghuber OC. Non-invasive pressure support ventilation in
patients with respiratory failure due to severe acute cardiogenic pulmonary edema.
Respiration 2004; 71: 144-151.
54. Jolliet P, Abajo B, Pasquina P, Chevrolet JC. Non-invasive pressure support ventilation in
severe community-acquired pneumonia. Intensive Care Med 2001; 27: 812-821.
55. Krall SP, Zubrow MT, Silverman ME. Success in using non-invasive mechanical
ventilation is predicted by patient pathophysiology. A retrospective review of 199
patients. Del Med J 1999; 71: 213-220.
56. Mollica C, Brunetti G, Buscajoni M, et al. Non-invasive pressure support ventilation in
acute hypoxemic (non hypercapnic) respiratory failure. Observations in respiratory
intermediate intensive care unit. Minerva Anestesiol 2001; 67: 107-115.
57. Rocco M, Conti G, Antonelli M, et al. Non-invasive pressure support ventilation in
patients with acute respiratory failure after bilateral lung transplantation. Intensive Care
Med 2001; 27: 1622-1626.
58. Jiang JS, Kao SJ, Wang SN. Effect of early application of biphasic positive airway
pressure on the outcome of extubation in ventilator weaning. Respirology 1999; 4: 161165.
59. Jardine E, O'Toole M, Paton JY, Wallis C. Current status of long term ventilation of
children in the United Kingdom: questionnaire survey. BMJ 1999; 318: 295-299.
60. Villa M, Pagani J, Ambrosio R, Ronchetti R, Bernkopf E. Mid-face hypoplasia after longterm nasal ventilation. Am J Respir Crit Care Med 2002; 166: 1142-1143.
61. Fiorenza D, Vitacca M, Clini E. Hospital monitoring, setting and training for home non
invasive ventilation. Monaldi Arch Chest Dis 2003; 59: 119-122.
ARTICLE
High-frequency oscillatory ventilation —
a clinical approach
Pediatric Critical Care Medicine, Duke University Children’s Hospital, Durham, North
Carolina, USA
Donna S Hamel, RRT, RCP, FAARC
Ira M Cheifetz, MD, FCCM, FAARC
Since its inception over a decade ago, HFOV has become an increasingly utilised and effective strategy for the
treatment of acute lung injury and acute respiratory distress syndrome. During HFOV, the lungs are recruited
and stabilised to avoid the cyclic stretch and shear exerted on the alveoli which occur during conventional
ventilation by repeated alveolar collapse and re-expansion. Patients with deteriorating gas exchange despite
increasing ventilatory settings can be successfully managed with HFOV as it provides significant lung
protection. However, as with any mode of ventilation, management strategies must be designed to minimise (or
eliminate) ventilator-induced lung injury based on a patient’s pathophysiology.
Mechanical ventilatory strategies have evolved
dramatically over the past decade. The deleterious
effects of mechanical ventilation have been widely
SAJCC
33. Sidhu US, Behera D. Non invasive ventilation in COPD. Indian J Chest Dis Allied Sci
2000; 42: 105-114.
49. L'Her E, Moriconi M, Texier F, et al. Non-invasive continuous positive airway pressure in
acute hypoxaemic respiratory failure – experience of an emergency department. Eur J
Emerg Med 1998; 5: 313-318.
July 2005, Vol. 21, No. 1
32. Rizvi N, Mehmood N, Hussain N. Role of Bi-pap in acute respiratory failure due to acute
exacerbation of COPD. J Pak Med Assoc 2001; 51: 414-417.
48. Hore CT. Non-invasive positive pressure ventilation in patients with acute respiratory
failure. Emerg Med (Fremantle) 2002; 14: 281-295.
studied and are universally recognised.1-7 When high
peak airway pressures, elevated mean airway
pressures, excessive FiO2, and/or large tidal volumes
15
pg 10-24 q5
8/8/05
2:10 PM
Page 16
are necessary to maintain adequate gas exchange,
patients are at risk of developing ventilator-associated
lung injury.8,9 High-frequency ventilation was first
introduced in the late 1970s as an alternative method of
mechanical ventilation designed specifically to reduce
the complications associated with conventional
mechanical ventilation.
PIP vent
PIPalv
PAWalv
July 2005, Vol. 21, No. 1
SAJCC
∆P vent
16
High-frequency ventilation is defined as a delivered
tidal volume that is less than anatomical dead space
and delivered at a high frequency rate (> 120 breaths
per minute for adults, > 150 breaths per minute for
infants and children). This relationship between dead
space and ventilation was discussed as early as 1915
when Henderson and colleagues theorised that gas
exchange sufficient to support life could be achieved
even at tidal volumes considerably less than dead
space.10-12 However, it was not until the 1970s that
interest in a clinical application of high-frequency
ventilation emerged. Studies during the 1970s clearly
demonstrated in animal models of acute lung injury
that adequate alveolar ventilation could be achieved
with tidal breaths smaller than anatomical dead space
and accelerated breathing frequencies.12,13 When
ventilating with these extremely small tidal volumes,
peak airway pressures are dramatically reduced leading
to the belief that high-frequency ventilatory approaches
minimise the adverse effects of volutrauma,
barotrauma, and stretch injury associated with
conventional ventilation.14-17
The two most common forms of high-frequency
ventilation are high-frequency jet ventilation (HFJV)
and high-frequency oscillatory ventilation (HFOV).
HFJV is most commonly performed via the Life Pulse
ventilator (Bunnell Inc., Salt Lake City, Utah, USA),
which delivers pulses of gas at a high velocity through
an orifice at a frequency of 240 - 660 breaths per
minute. The small high-velocity breaths and fast rates
coupled with passive exhalation provide an effective
means for carbon dioxide elimination at reduced peak
inspiratory pressures. Positive end-expiratory pressure
and ‘sigh’ breaths are provided with a conventional
ventilator used in tandem with the jet ventilator. Mean
airway pressure during jet ventilation is achieved
indirectly by the manipulation of other ventilatory
parameters. While the Life Pulse high-frequency jet
ventilator is an effective means for ventilating infants
and small children, it is not FDA approved to support
larger paediatric and adult patients.
HFOV effectively provides support to infants, children
and adults with acute lung injury. HFOV allows the
clinician to directly set and manipulate the mean
airway pressure (PAW). During HFOV, the PAW is set to
achieve an optimal lung volume. High-frequency
oscillation allows the clinician to open the lung and
keep it open, thus improving outcomes by decreasing
the shear forces associated with the repetitive opening
of collapsed alveoli.18 Tidal volumes (i.e. oscillations)
∆PalvV
PAW vent
PEEPalv
PEEP vent
Fig. 1. Pressure attenuation during HFOV. The pressure
generated by the high-frequency oscillator attenuates as gas
moves along the oscillator circuit, endotracheal tube, and
conducting airways.
are then superimposed on the PAW allowing for the
utilisation of higher mean airway pressures at lower
peak airway pressures. A key concept of highfrequency ventilation (both oscillation and jet) is that
the swing from maximal to minimal airway pressure is
attenuated as gas flow progresses from the ventilator to
the alveoli (Fig. 1). This may also be described as an
attenuation of the peak-to-trough swing across the
mean airway pressure. HFOV is an attractive
alternative to conventional mechanical ventilation for
the respiratory management of a wide range of
critically ill patients with acute lung injury.
Theory of gas exchange during
HFOV
While the gas exchange mechanisms during
conventional mechanical ventilation are convection
ventilation or ‘bulk flow’, gas exchange during HFOV is
enhanced by other mechanisms. Even with the small
tidal volumes of HFOV, direct alveolar ventilation may
occur to short path length units that branch from the
primary airways. However, this only accounts for a
small component of the gas exchange that occurs
during HFOV.
Molecular diffusion is speculated to be a major
contributor to gas exchange during oscillatory
ventilation. Molecular diffusion describes gas
exchange across the alveolar-capillary membrane and
contributes to the transport of both oxygen and carbon
dioxide in the gas phase near the membrane. In 1984,
Slutsky and colleagues11 theorised that the gas
exchange mechanism during HFOV was caused by the
coupled effects of convection and molecular diffusion.
It is speculated that this is due to an increase in
turbulence of the molecules during high-frequency
oscillation.19 In that same year, Chang and colleagues20
determined that a convective mechanism may
predominate with the increased tidal volume at lower
ventilatory rates, while a diffusive mechanism may
pg 10-24 q5
8/8/05
2:12 PM
Page 18
July 2005, Vol. 21, No. 1
SAJCC
predominate with the decreased tidal volume at higher
frequencies.
Taylor dispersion is also proposed as a significant
contributor to gas exchange. Taylor dispersion occurs
when a high velocity of gas travels down the centre of a
tube, leaving the molecules on the periphery unmoved.
When the high-velocity flow stops, gas molecules then
diffuse evenly along the tube (Fig. 2).21-23 A variation of
this theory describes an asymmetrical velocity profile.
During inspiration, the high-frequency pulse creates a
‘bullet’-shaped profile with the central molecules
moving further down the airway than those molecules
found on the periphery of the airway (i.e. ‘two steps
forward’ approach) (Fig. 3).22,23
Fig. 4. The Pendeluft effect suggests that at high
frequencies, gas distribution becomes strongly influenced
by time constant inequalities. Gas from fast units (i.e.
short time constants) will empty into the slow units (i.e.
long time constants).
with cardiogenic mixing, in which the heartbeat adds
to the gas mixing, contribute to the effective gas
exchange abilities of HFOV.23
18
HFOV specifications
Fig. 2. Taylor dispersion occurs when a high velocity of gas
travels down the centre of a tube, leaving the molecules on
the periphery unmoved. When the high-velocity flow stops,
gas molecules then diffuse evenly along the tube.
Fig. 3. Depiction of an asymmetrical velocity profile where,
during inspiration, the high-frequency pulse creates a ‘bullet’shaped profile with the central molecules moving further
down the airway than those molecules found on the periphery
of the airway pattern.
Still another theory was proposed by Lehr et al., who
attributed effective gas exchange during HFOV to the
Pendeluft effect.24 At high frequencies, gas distribution
becomes strongly influenced by time-constant
inequalities. Gas from fast units (i.e. short time
constants) will empty into the slow units (i.e. long time
constants) (Fig. 4).
It is likely that a combination of these mechanisms
(rather than a single mechanism) is responsible for the
effectiveness of gas exchange during HFOV.20 It is
possible that all of these proposed mechanisms coupled
Currently, the most commonly used devices to perform
HFOV are the SensorMedics 3100A and 3100B
ventilators (Viasys Healthcare, Yorba Linda, California,
USA). These ventilators are electronically controlled
piston-diaphragm high-frequency ventilators. The
3100A is designed to ventilate all patients regardless of
weight; however, carbon dioxide elimination may be
ineffective for some ‘larger’ patients. The 3100B
oscillator is FDA approved only for patients weighing
more than 35 kilograms.
The 3100A utilises bias flow rates of 0 to 40 l/min and is
capable of delivering mean airway pressures between 3
and 45 cm H2O. The 3100B has an increased bias flow
ability (0 - 60 l/min) and can deliver higher mean
airway pressures (3 - 55 cm H2O). Inspiratory times
range between 33% and 50% for the 3100A and
between 30% and 50% for the 3100B. Both oscillators
utilise similar frequency (3 - 15 hertz) and amplitude
(8 - 90 cm H2O) ranges; however, the lower bias flow
ranges of the 3100A often make it difficult to achieve
the higher mean airway pressures and larger amplitude
requirements for ‘larger’ patients.
Physiology of gas exchange
During HFOV, oxygenation and ventilation are
decoupled.25 Oxygenation is primarily a function of
FiO2 and PAW. Mean airway pressure is used to inflate
the lung and optimise the alveolar surface area for gas
exchange (i.e. PAW equals lung volume).23 PAW during
HFOV is created by a continuous bias flow of gas past
a resistance (inflation) of a balloon on the mean airway
pressure valve. Therefore, the PAW is changed by
adjusting the bias flow or the inflation of the balloon
control valve (PAW adjust knob). Simply stated, PAW
during HFOV is a clinician set value, not a byproduct of
other variables. In fact, the PAW of the oscillator
pg 10-24 q5
8/8/05
2:14 PM
Page 20
without the piston moving is a continuous positive
airway pressure (CPAP) system.
July 2005, Vol. 21, No. 1
SAJCC
As with conventional ventilation, carbon dioxide
elimination during HFOV is achieved by adjusting the
minute ventilation. However, during conventional
ventilation minute ventilation is defined as tidal volume
times frequency (Vt x f), whereas during HFOV, minute
ventilation is equal to Vt1.5-2.5 x f.26,27 Therefore, changes
in tidal volume delivery have the most significant effect
on carbon dioxide elimination.
20
lesions who have an oxygen index of greater than 13 on
two consecutive arterial blood gases within a 6-hour
period should also be considered candidates for HFOV.
Careful consideration should be employed when
intracranial hypertension is present. The potential
benefit of improved gas exchange at lower airway
distending pressures should be carefully weighed
against the risk of further increasing intracranial
pressures.
Initiation of HFOV
Tidal volume delivery during HFOV is defined as the
gas displaced by the movement of the oscillatory
piston. The amount of piston movement is a function
of delta P (i.e. amplitude), frequency, and per cent
inspiratory time (% Ti).25 The primary control of carbon
dioxide elimination is the delta P.28 Delta P displayed
on the front panel is produced by adjustment of the
power setting. The delta P produces a stroke volume
(also referred to as amplitude). The amplitude itself is
created by the distance that the piston moves resulting
in volume displacement and a visible patient ‘chest
wiggle’ (i.e. oscillation).
When preparing patients for conversion to HFOV
always consider the underlying pathology and
thoroughly review the chest radiographs and arterial
blood gases. It is also important to know the most
recent mean airway pressure obtained during
conventional ventilation. If the patient’s pH is less than
7.25, consider buffering with sodium bicarbonate
(NaHCO3) before initiating HFOV. It should be noted
that the use of sodium bicarbonate to buffer acidosis in
this situation remains controversial. Growing evidence
in the literature discourages this practice.29
The secondary control of carbon dioxide elimination is
the frequency setting. The power controls the force
with which the piston moves, and the frequency
controls the time allowed (distance) for the piston to
move. Therefore, the lower the frequency the greater
the volume displaced; and the higher the frequency, the
smaller the volume displaced (Fig. 5). The % Ti also
controls the time for movement of the piston and can
therefore assist in carbon dioxide elimination as well.
Increasing the % Ti is generally a technique used for
ventilating larger patients.
Most patients should have a functional arterial line.
Pulse oximetry is absolutely essential. Transcutaneous
oxygen and carbon dioxide monitoring is extremely
useful. As patient size increases, the reliability of
transcutaneous oxygen monitoring decreases.
However, with newer technology available
transcutaneous carbon dioxide monitoring is a very
reliable trend monitor in most patients regardless of
size. A central venous line may be helpful. A
pulmonary artery catheter is not necessary and, in fact,
is rarely utilised for this population of patients.
Sedation is required for most infants, and some may
require paralysis. Essentially all paediatric and adult
patients require sedation, and most will require
paralysis at least initially. However, once the patient
has entered the weaning phase, a trial without
neuromuscular blockade should be done.
Fig. 5. Frequency and tidal volume during HFOV. The power
controls the force with which the piston moves, and the
frequency controls the time allowed (distance) for the piston
to move. Therefore, the lower the frequency the greater the
volume displaced; and the higher the frequency, the smaller
the volume displaced.
Clinical indications
Patients with diffuse alveolar diseases, such as acute
respiratory distress syndrome (ARDS), acute lung injury
(ALI), bronchiolitis and air leak syndrome, may benefit
from the use of HFOV. Most patients who require high
ventilatory settings during conventional ventilation
could potentially benefit from HFOV. Consider HFOV
for patients with oxygen requirements greater than
0.60, peak inspiratory pressures greater than 32 cm
H2O, and mean airway pressures in excess of 15 cm
H2O. Patients without cyanotic congenital cardiac
The patient should be suctioned before initiation of
HFOV to assure the removal of excess secretions.
Since de-recruitment may occur with suctioning,
suctioning should be based on the patient’s overall
clinical status. Closed suction catheter systems can be
used; however, it is essential to completely remove the
suction catheter tip from the endotracheal tube (ETT)
at the completion of suctioning. When catheters
remain in the ETT, the delivered amplitude will be
attenuated and a decrease in the ‘chest wiggle factor’
will be seen. Additionally, if a disconnect between the
suction adaptor and the ETT occurs, there may be
sufficient pressure to prevent the low pressure alarm
from sounding. Oximetry and transcutaneous
monitoring have the added benefit of notifying the
clinician of adverse patient effects secondary to circuit
disconnects.
pg 10-24 q5
8/8/05
2:16 PM
Page 22
July 2005, Vol. 21, No. 1
SAJCC
Before transition from conventional to high-frequency
ventilation, the clinician should ensure that the patient
has adequate intravascular volume and cardiac output.
Intravascular volume loading may be required on
initiation of HFOV secondary to the associated increase
in intrathoracic pressure.30-33 When available, the
central venous pressure (CVP) should be monitored to
assist in intravascular fluid management. Patients
often require a low-dose inotrope infusion to augment
cardiac output during the transition to HFOV.
22
On initiating HFOV, the FiO2 should be set at 1.0. The
bias flow should be set at 18 l/min or more for neonatal
and paediatric patients. A 30 - 40 l/min bias flow is
often required for larger paediatric and adult patients.
An adequate bias flow is necessary to assure
replenishment of the oxygen supply to the endotracheal
tube and for optimal carbon dioxide removal from the
circuit. If the bias flow is inadequate, circuit dead
space increases and carbon dioxide removal can be
impaired. The bias flow should be increased in
increments of 5 l/min when carbon elimination is
inadequate despite appropriate amplitude and
frequency adjustments.
The mean airway pressure on the oscillator should be
set at 4 - 8 cm H2O above the level generated on the
conventional mechanical ventilator for patients with
diffuse alveolar disease.34-37 This increase is required
secondary to the pressure attenuation which can occur
along the oscillator circuit, endotracheal tube and
airways. Additionally, the increased mean airway
pressure is intended to augment lung recruitment in
patients with acute alveolar injury (i.e. acute lung injury
or acute respiratory distress syndrome). The frequency
should be set according to the patient’s weight and age
(Table I). The % Ti should be set initially at 33% on the
3100A and 30% on the 3100B. The power setting
control should be set at 6 and then adjusted to meet the
desired amplitude. The power setting needed to
provide an adequate amplitude (and chest oscillation) is
dependent on the patient’s size, weight and pulmonary
compliance.
When titrating the power setting to achieve the optimal
amplitude, the clinician should observe the patient for
adequate ‘chest wiggle’ and therefore adequate chest
oscillation. The amplitude is considered appropriate
Table I.
Weight (kg)
1.5 - 2.0
2.0 - 5.0
5.0 - 12.0
12.0 - 20.0
21.0 - 30.0
> 30.0
Suggested high-frequency
oscillatory frequency settings based
on patient weight
Suggested frequency (hertz)
12
10
9
8
7
6
when the patient has a visible oscillation from the chest
to the upper thighs. Transcutaneous carbon dioxide
monitoring is also useful for setting the amplitude. In
larger patients, the transcutaneous values may not be
identical to the arterial blood gas values; however,
transcutaneous monitoring can be used successfully for
the trending of gas exchange in most patients.
A decrease in chest oscillation is a clinical sign that
pulmonary compliance has decreased. If a decrease in
chest oscillation is noted, assess the airway to
determine if there is an obstruction, then consider
endotracheal tube suctioning. A unilateral reduction in
chest oscillation indicates that the endotracheal tube
may be in the right mainstem bronchus or a
pneumothorax may be present. Check the
endotracheal tube position and obtain a chest
radiograph. Always reassess the chest oscillation
following any change in patient position.
Patients with air leak syndrome require a low lung
volume strategy even with HFOV. Therefore, a
relatively lower mean airway pressure should be used.
The PAW setting in unilateral air leak syndrome is
dependent on the inflation of the unaffected lung. The
clinician should accept less than optimal arterial blood
gas values until the air leak resolves. Accept oxygen
saturations of 85 - 90% with incremental increases in
the FiO2 as needed. Atelectasis is a possibility when
ventilating with a low lung volume strategy.
Hypercapnia with a pH of 7.25 or greater should be
acceptable.38,39 When adequate oxygenation and
ventilation are achieved, decrease the mean airway
pressure and amplitude. A higher FiO2 must often be
accepted with air leak syndrome to provide for the
lowest airway pressures and thus provide optimal lung
protection. Once the chest tube air leak has resolved
for least 24 hours, gently recruit the collapsed lung and
begin weaning.
HFOV management strategies
Inadequate oxygenation requires adjustment of the
mean airway pressure. PAW should be adjusted until
optimal lung volume is achieved. Adjustments in PAW
should generally be performed in increments of 1 - 2 cm
H2O for infants and children and 2 - 3 cm H2O for adult
patients. Lung volume is considered optimal when
lung expansion is at the 9th thoracic vertebra (T9) on a
chest radiograph. It is at this level that there should be
a resultant increase in oxygen saturation which will
allow for the reduction of FiO2. To optimise lung
recruitment, consider a sustained inflation (volume
recruitment) manoeuvre. Sustained inflation
manoevres allow for a more rapid increase in lung
volume compared with a gradual increase in the mean
airway pressure.40-42 Sustained inflation manoeuvres
may be performed while on the HFOV by increasing the
PAW by 5 - 8 cm H2O for 30 - 40 seconds while the
piston is stopped. At completion of a volume
pg 10-24 q5
8/8/05
2:16 PM
Page 23
recruitment manoeuvre, the mean airway pressure
should be returned to the previous setting.
A decrease in chest oscillation (‘chest wiggle’) is a
clinical sign that pulmonary compliance has decreased.
The assessment of a change in chest oscillation is
discussed in more detail under ‘Initiation of HFOV’.
In larger patients with an unacceptable PaCO2, the % Ti
provides an additional means for improving carbon
dioxide elimination. While it is recommended that the
% Ti be set at 30% when utilising the 3100B and 33%
when utilising the 3100A, if the amplitude has been
maximised and the frequency has been minimised,
increase the inspiratory time towards 50%. Increasing
the % Ti will increase the delivered tidal volume and,
therefore, should improve ventilation. Additionally, for
patients with cuffed endotracheal tubes, minimally
deflating the cuff may improve ventilation by allowing
for passive exhalation around the endotracheal tube
throughout the entire breath cycle (Fig. 6).
Patient assessment
Obtain an initial chest radiograph approximately 1 hour
after the initiation of HFOV. Then obtain a chest
radiograph every 12 hours for the first 24 hours of
o2
SAJCC
Managing carbon dioxide elimination is primarily
performed by manipulating the power setting control.
To reduce the PaCO2, increase the power setting
control (i.e. amplitude) in 3 - 5 cm H2O increments.
Additionally, if the amplitude has been increased by
10 - 20 cm H2O and there is a clinically inadequate
decrease in the PaCO2, decrease the set frequency. The
frequency should be manipulated in increments of 0.5 1 Hz. If the initial frequency is too high, unacceptable
PaCO2 levels may result. It is important to note that
PaCO2 may initially climb in large patients before it
stabilises and then decreases. Therefore, allow a 5 10-minute stabilisation period after each parameter
change. Permissive hypercapnia should be acceptable
for most patients.45
July 2005, Vol. 21, No. 1
When performing a sustained inflation manoeuvre, risks
do exist, such as haemodynamic instability and
pneumothorax. Always monitor the patient’s
haemodynamic status when manipulating the mean
airway pressure as perfusion must be matched to
ventilation for adequate oxygenation to be achieved. It
is also important to note that pulmonary vascular
resistance is increased with either atelectasis or
pulmonary overdistension.43,44 Therefore, the clinician
should utilise chest radiographs and pulse oximetry to
optimise lung recruitment while guarding against
overexpansion. If the chest radiograph demonstrates
optimal expansion, the FiO2 has been maximised and
oxygenation remains poor, increasing the % Ti to 50%
will raise the distal PAW closer to the proximal values.
Thus, increasing the % Ti will increase the effective
PAW. It is important to note that increasing the % Ti
will also increase the delivered tidal volume.
co2
o2
Fig. 6. Endotracheal tube air leak. During HFOV, passive
exhalation of gas around the endotracheal tube throughout
the entire ventilatory cycle occurs when the endotracheal
tube cuff is deflated. Care must be taken when deflating the
cuff to be sure that the oscillator can still maintain the set
mean airway pressure. To achieve this balance, the cuff is
often only minimally deflated.
HFOV. After the initial 24 hours, chest radiographs can
generally be obtained once daily. While obtaining the
chest radiograph, it is not necessary to stop the piston
or reposition the head. Do not remove the patient from
the oscillator and manually ventilate as this will not
provide the information necessary to manage the
oscillator as lung expansion will have changed.
Assessment of breath sounds during HFOV is difficult
and identifying cardiac sounds is nearly impossible. To
assess breath sounds it is not necessary to stop the
piston. Listen for the intensity and quality of sounds
throughout the chest. Breath sounds should be
symmetrical. Always take any changes in breath
sounds seriously. When a change is noted, stop the
piston for further evaluation. When the piston is
stopped the patient is on CPAP. Obtain a chest
radiograph if there is any concern. When assessing
cardiac sounds the piston must be stopped. Listen
quickly to the heart sounds and restart the piston.
Weaning and conversion to
conventional mechanical
ventilation
The initial approach to weaning should be a reduction
in the most toxic ventilatory parameter(s). Patients
with diffuse alveolar disease should begin with a
reduction in the FiO2. Once FiO2 has been reduced to
less than 0.60, begin weaning the mean airway
pressure. The PAW should be decreased in increments
of 1 - 2 cm H2O for oxygen saturations greater than
approximately 88% while maintaining adequate lung
volume. De-recruitment occurs much more slowly than
recruitment.17 In the event that lung volume is lost
during the process of weaning, adequate lung volume
can be quickly achieved with a sustained inflation
manoeuvre followed by an incremental increase in the
PAW.
23
pg 10-24 q5
8/8/05
2:16 PM
Page 24
July 2005, Vol. 21, No. 1
SAJCC
The frequency should be increased in increments of 0.5
- 1 Hz until it is returned to the appropriate rate based
on the patient’s age and weight. Once the appropriate
frequency is achieved, begin weaning the amplitude.
The amplitude should be decreased in increments of 3 5 cm H2O using the transcutaneous monitor as a guide.
The % Ti should be returned to 30% for 3100B patients
and 33% for patients ventilating with the 3100A before
conversion to conventional ventilation.
24
Once the lung process has stabilised, the oscillatory
support has been minimised and the arterial blood
gases have improved, consider transition to
conventional mechanical ventilation. While every
patient is different, consider changing when the FiO2 is
less than 0.40, the PAW is 14 - 20 cm H2O, and the
amplitude is less than 30 cm H2O. If the endotracheal
tube cuff was deflated during HFOV, consider reinflating it. Most patients make the transition to a
pressure-limited mode (i.e. decelerating inspiratory
flow) of ventilation with a peak inspiratory pressure less
than 30 cm H2O. The targeted tidal volume should be 6
ml/kg.2,46 The suggested FiO2 is less than or equal to
0.50 with a PEEP of approximately 10 cm H2O. The
respiratory rate should be at the appropriate
physiological rate for the patient’s age.
1. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-lung strategy on
mortality in acute respiratory distress syndrome. N Engl J Med 1998; 338: 347- 354.
2. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of
ventilator induced lung injury in acute respiratory distress syndrome. The multicenter
trial on Tidal Volume Reduction in ARDS. Am J Respir Crit Care Med 1998; 158: 18311838.
3. Kolobow T, Moretti MP, Fumagalli R, et al. Severe impairment in lung function induced
by high peak airway pressure during mechanical ventilation. Am Rev Respir Dis 1987;
135: 312-315.
17. Arnold JH, Hanson JH, Toro-Figuero LO, Gutierrez J, Berens RJ, Anglin DL. Prospective,
randomized comparison of high-frequency oscillatory ventilation and conventional
mechanical ventilation in pediatric respiratory failure. Crit Care 1994; 22: 1530-1539.
18. Rimensberger PC, Pristine G, Mullen BM, Cox PN, Slutsky AS. Lung recruitment during
small tidal volume ventilation allows minimal positive end-expiratory pressure without
augmenting lung injury. Crit Care Med 1999; 27: 1940-1945.
19. Abbasi S, Bhutani VK, Spitzer AR, Fox WW. Pulmonary mechanics in preterm neonates
with respiratory failure treated with high-frequency oscillatory ventilation compared with
conventional mechanical ventilation. Pediatrics 1991; 87: 487-493.
20. Chang H. Mechanisms of gas transport during ventilation by high frequency oscillation. J
Appl Physiol 1984; 56: 553-563.
21. Fredberg JJ. Augmented diffusion in the airways can support pulmonary gas exchange. J
Appl Physiol 1980; 49: 232-238.
22. Haselton FR, Scherer PW. Bronchial bifurcations and respiratory mass transport. Science
1988; 208: 69-71.
23. Bouchet JC, Godard J, Claris O. High-frequency oscillatory ventilation. Anesthesiology
2004; 100: 1007-1012.
24. Lehr JL, Butler JP, Westerman PA, Zatz SL. Drazen JM. Photographic measurement of
pleural surface motion during lung oscillation. J Appl Physiol 1985; 59: 623-633.
25. Schindler M, Seear M. The effects of lung mechanics on gas transport during high
frequency oscillation. Pediatr Pulmonol 1991; 11: 335-339.
26. Scalfaro P, Pillow JJ, Sly PD, Cotting J. Reliable tidal volume estimates at the airway
opening with an infant monitor during high frequency oscillatory ventilation. Crit Care
Med 2001; 29: 1925-1930.
27. Jaeger MJ, Kurzweg UH, Banner MJ. Transport of gases in high frequency ventilation.
Crit Care Med 1984; 12: 708-710.
28. Slutsky AS, Kamm RD, Rossing TH, et al. Effects of frequency, tidal volume and lung
volume on CO2 elimination in dogs by high frequency (2-30Hz), low tidal volume
ventilation. J Clin Invest 1981; 68: 1475-1484.
29. Laffey JG, Engelberts D, Kavanagh BP. Buffering hypercapnic acidosis worsens acute
lung injury. Am J Respir Crit Care Med 2000; 161: 141-146.
30. Traverse JH, Korvenranta H, Adams EM, Goldthwait DA, Carlo WA. Impairment of
hemodynamics with increasing mean airway pressure during high frequency oscillatory
and jet ventilation. Pediatr Res 1988; 23: 628-631.
31. Traverse JH, Korvenranta H, Adams EM, Goldthwait DA, Carlo WA. Cardiovascular
effects of high frequency oscillatory and jet ventilation in normal and septic piglets. Biol
Neonate 1989; 96: 1400-1404.
32. Osiovich HC, Suguihara C, Goldberg RN, Hehre D, Martinez O, Bancalari E.
Hemodynamic effects of conventional and high frequency oscillatory ventilation in
normal and septic piglets. Biol Neonate 1991; 59: 244-252.
33. Kinsella JP, Gerstmann DR, Clark RH, et al. High frequency oscillatory ventilation versus
intermittent mandatory ventilation: Early hemodynamic effects in the premature baboon
with hyaline membrane disease. Pediatr Res 1991; 29: 160-166.
34. Arnold JH. High-frequency ventilation in the pediatric intensive care unit. Pediatr Crit
Care Med 2000; 1: 93-99.
35. Goddon S, Fujino Y, Hromi JM, Kacmarek RM. Optimal mean airway pressure during
high-frequency oscillation: predicted by the pressure-volume curve. Anesthesiology 2001;
94: 862-869.
4. Papadakos PJ, Apostolakos MJ. High-inflation pressure and positive end expiratory
pressure. Injurious to the lung? Yes. Crit Care Clin 1996; 12: 627-634.
36. Van Genderingen HR, van Vught AJ, Duval EL. Markhorst DG, Jansen JR. Attenuation of
pressure swings along the endotracheal tube is indicative of optimal distending pressure
during high-frequency oscillatory ventilation in a model of acute lung injury. Pediatr
Pulmonol 2002; 33: 429-436.
5. Marshall RP. Current strategies for mechanical ventilation in acute lung injury. Hosp Med
2000; 61: 678-679.
37. Arnold JH. High-frequency ventilation in the pediatric intensive care unit. Pediatr Crit
Care Med 2000; 1: 93-99.
6. Tsuno K, Prato P, Kolobow T. Acute lung injury from mechanical ventilation at moderately
high airway pressures. J Appl Physiol 1990; 69: 956-961.
38. Clark RH, Slutsky AS. Gertsmann DR. Lung protective strategies of ventilation in the
neonate: What are they? Pediatrics 2000; 1: 112-114.
7. Thompson WK, Marchak BE, Froese AB, Bryan AC. High-frequency oscillation compared
with standard ventilation in pulmonary injury model. J Appl Physiol 1982; 52: 543-548.
39. Slutsky A. Mechanical Ventilation: American College of Chest Physician's Consensus
Conference. Chest 1993; 104: 1833-1859.
8. Marini JJ. Microvasculature in ventilator-induced lung injury: target or cause? Minerva
Anesthesiol 2004; 70: 167-173.
40. Bond DM, Froese AB. Volume recruitment maneuvers are less deleterious than persistent
low lung volumes in the atelectasis-prone rabbit lung during high-frequency oscillation.
Crit Care Med 1993; 21: 402-412.
9. Simonson DA, Adams AB, Wright LA, Dries DJ, Hotchkiss JR, Marini JJ. Effects of
ventilatory pattern on experimental lung injury caused by high airway pressure. Crit Care
Med 2004; 32: 781-786.
10. Gerstmann D. Major benefit of small tidal volumes during high-frequency ventilation. Crit
Care 2003; 31: 328-329.
11. Slutsky AS. Drazen JM. Ventilation with small tidal volumes. N Engl J Med 2002; 347:
630-631.
12. Wetzel RC, Gioia FR. High frequency ventilation. Pediatr Clin North Am 1987; 34: 15-38.
13. Martinon-Torres F, Rodriguez-Nunez A, Matinon-Sanchez JM. Advances in mechanical
ventilation. N Engl J Med 2001; 345: 1133-1134.
14. Von der Hardt K, Kandler MA, Fink L, et al. High frequency oscillatory ventilation
suppresses inflammatory response in lung tissue and microdissected alveolar
macrophages in surfactant depleted piglets. Pediatr Res 2004; 55: 339-346.
15. Imai Y, Slutski AS. Comparison of lung protection strategies using conventional and
high-frequency oscillatory ventilation. J Appl Physiol 2001; 91: 1836-1844.
16. Gerstmann DR, Wood K, Miller A, et al. The Provo multicenter early high-frequency
oscillatory ventilation trial: improved pulmonary and clinical outcome in respiratory
distress syndrome. Pediatrics 1996; 98: 1044-1057.
41. Byford LJ, Finkler JH, Froese AB. Lung volume recruitment during high frequency
oscillation in atelectasis prone rabbits. J Appl Physiol 1988; 64: 1607-1614.
42. Ferguson ND, Chiche JD, Kacmarek RM, et al. Combining high-frequency oscillatory
ventilation and recruitment maneuvers in adults with early acute respiratory distress
syndrome: The Treatment with Oscillation and an Open Lung Strategy (TOOLS) Trial
pilot study. Crit Care Med 2005; 33: 479-486.
43. Cheifetz IM, Meliones JN. Hemodynamic effects of high-frequency oscillatory ventilation:
a little volume goes a long way. Crit Care Med 2000; 28: 282-284.
44. Zellers TM, Luckett PM. Cardiopulmonary interactions. In: Levin DL, ed. Pediatric
Intensive Care. Vol. 1. 2nd ed. New York: Churchill Livingstone, Quality Medical
Publishing, 1997: 1813.
45. Hickling KG. Low volume ventilation with permissive hypercapnia in the adult
respiratory dress syndrome. Clin Intensive Care 1992; 3: 67-78.
46. The Acute Respiratory Distress Network. Ventilation with lower tidal volumes as
compared with traditional tidal volumes for acute lung injury and the acute respiratory
distress syndrome. N Engl J Med 2000; 342: 1301-1308.